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Defensins in Systemic Lupus Erythematosus
Author(s) -
Froy Oren,
Sthoeger Zev M.
Publication year - 2009
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.2009.04622.x
Subject(s) - immunology , innate immune system , pathogenesis , immune system , acquired immune system , defensin , inflammation , degranulation , medicine , autoimmune disease , systemic lupus erythematosus , lupus erythematosus , secretion , antibody , disease , biology , receptor , microbiology and biotechnology , endocrinology , antimicrobial
Systemic lupus erythematosus (SLE) is an autoimmune disease, resulting in inflammation and tissue damage. The precise etiology for SLE is so far unknown. It has been shown that the innate immunity plays a role in SLE pathogenesis. The innate immune system confers broad protection against pathogens by the secretion of broad‐spectrum antibacterial and immunomodulatory substances named defensins. Recently, α‐defensin, the products of neutrophils have been found to be upregulated at the mRNA and protein levels in SLE patients. In addition, increased antidefensin antibodies were found in sera of patients with SLE, but these levels decreased after therapy with corticosteroids. These recent findings suggest a role for defensins in the pathogenesis of SLE. Thus, activation and degranulation of neutrophils leads to α‐defensin secretion in SLE patients. Given their immunomodulatory role, α‐defensin secretion might activate the adaptive immune system leading to the stimulation of the immune system, as is manifested in SLE.